Toxicity of environmental Gesagard to goldfish may be connected with induction of low intensity oxidative stress in concentration- and tissue-related manners.

Prometryn is a selective herbicide commonly used in agriculture as the commercial preparation, Gesagard. Goldfish (Carassius auratus) exposure for 96h to 0.2, 1, or 5mgL(-1) Gesagard 500FW (corresponding to 0.1, 0.5, and 2.5mgL(-1) of prometryn) on indices of oxidative stress (lipid peroxides, protein carbonyls, and thiol content) and activities of antioxidant and related enzymes in gills, liver, and kidney was studied. Gills appeared to be the most resistant to Gesagard treatment, reacting to only the highest concentration of herbicide with enhanced levels of low molecular mass thiols and activities of glutathione S-transferase (GST) and glutathione reductase. Goldfish exposure to 0.2-5mgL(-1) Gesagard resulted in enhancement of carbonyl protein level and activity of superoxide dismutase (SOD), but reduced the lipid peroxide (LOOH) content and activity of glutathione peroxidase in liver. Kidney appeared to be the main target organ of Gesagard toxicity, showing the greatest number of parameters affected even under low concentrations of herbicide. An increase in the content of L-SH and activity of SOD was accompanied with decreased activities of catalase, GST, and glucose-6-phosphate dehydrogenase and reduced levels of LOOH in kidney of Gesagard treated fish. The treatment also induced various histological changes in goldfish liver and kidney which could be related to their dysfunction. The present study indicates that Gesagard induced oxidative stress of differing intensities in the three goldfish tissues and demonstrated that kidney would be the best target organ to analyze, reveal, and monitor Gesagard effects on fish.